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Diabetic ketoacidosis and
hyperosmolar hyperglycaemic state
Section 4 | Part 2 of 2
Curriculum Module III6 | Short-term complications
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What is DKA?
Absolute or relative insulindeficiency
Increase in counter-regulatoryhormones
Breakdown of fat and muscle
Biochemical triadhyperglycaemiaketoacids
metabolic acidosis
High blood glucose, ketones, acidosisand dehydration
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Incidence of DKA
Varies
Death mainly from cerebral oedema
Most common at onset in type 1diabetes
Recurrent episodes Can occur in type 2 diabetes
Kitabchi et al 2001, Joslin 2005
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DKA cause or trigger
Incidence
New-onset diabetes 5-40%
Acute illness 10-20%
Insulin omission/non-adherence 33%
Infection 20-38%
Heart attack, stroke,pancreatitis
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Insulin deficiency
Glucose uptake Lipolysis
Hyperglycaemia Gluconeogenesis
Glycerol Free fattyacids
Ketogenesis
Ketonemia
KetonuriaOsmotic diuresis
Urinary water losses
Electrolyte
depletion
Dehydration
Acidosis
Diabetic ketoacidosis
Adapted from Davidson 2001
Glucosuria
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Ketones
Used as fuel when calories arerestricted
Physiological ketosis when fastingor with prolonged exercise
Insulin deficiency lypolysis andketone production acidosis
beta-hydroxybutyrateacetoacetate
acetone
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Ketones
Beta-hydroxybutyratepredominant not detected by
test strips or acetone tablets
Ketoacidosis may be presentwithout detectable urinary ketones
Blood ketone testing may enableearly identification of DKA
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Earlier clinical symptoms andsigns of DKA
Polyuria
Polydipsia
Polyphagia
Tiredness
Muscle cramps
Flushed facial appearance
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Later clinical symptoms and signsof DKA
Weight loss
Nausea and vomiting
Abdominal pain
Dehydration
Acidotic breath
Hypotension Shock
Altered consciousness
Coma
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DKA investigations
Immediate for diagnosis Capillary blood glucose, urinary
glucose and ketones
Urgent for assessment and treatment Blood glucose Blood gases Electrolytes, urea, creatinine WBC
Consider Cardiac monitor Blood culture, urine culture Chest X-ray
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DKA laboratory findings
Blood glucose >14mmol/L (252mg/dL)
Ketones Urine: moderate to large
Blood: >3mmol/L
Osmolality Increased high blood glucose andurea/creatinine, dehydration
Electrolytes Low/normal Na+ and Cl-
Low/normal/high K+(often misleading)
Low HCO3 (normal 23-31)
Anion gap >10 mild
>12 moderate to severe
Blood gases pH
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DKA treatment
Rehydration 1. Correct shock with bolus saline
2. Rehydration rate depends on clinicalstatus, age and kidney function
Normal saline (0.9%) for resuscitationand rehydration initially
Glucose/saline solution when glucosearound 14 mmol/L (252mg/dL)
Rehydrate steadily over 48 hours
3. Consider NG tube
Potassium Essential after resuscitation and whenurine output confirmed
Kitabchi et al 1976
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DKA treatment
Insulin Infusion: 0.1 units/kg/hour afterresuscitation, saline established and BGfalling
Rate should be increased by 10-20% if
glucose not fallen by 2-3 mmol/L (45-54mg/dL) over first hour
Monitoring BG, BP, urine output and hourlyneurological status
Blood gases and electrolytes 2-hourlyinitially
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DKA complications
Hypoglycaemia +/- hypokalaemia
Acidosis not improving consider
continuing dehydration orinfection
Aspiration pneumonia
Headache +/- falling level ofawareness consider cerebraloedema and urgent treatmentwith Mannitol
Joslin 2005
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DKA recovery
Rapid improvement
Continue IV insulin while ketosis
present Oral intake when possible
Rapid-acting insulin 30-60 minutesbefore discontinuing IV insulin
Usual insulin regimen
Consider drinks and food containingpotassium
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What is HHS?
Ketosis may be present
Coma not always present
Primarily in older peoplewith/without history of type 2diabetes
Always associated with severedehydration and hyperosmolarstate
Develops over weeksKitabchi et al 2001
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HHS incidence and features
0.5% of primary diabetes hospitaladmissions
~15% mortality rate
Can occur in type 1 diabetes and
younger people
Kitabchi et al 2001
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HHS key features
Marked hyperglycaemia
Hyperosmolarity
Absence of severe ketosis
Altered mental awareness
Joslin 2005
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HHS causes or triggers
Booth 2001
Incidence
Infection 40-60%
New-onset diabetes 33%
Acute illness 10-15%
Medicines, steroids
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Signs and symptoms of HHS
Initially polyuria andpolydipsia
Altered mental status
Profound dehydration
Precipitating factors
d
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HHS biochemical findings
Jones 2001
Blood glucose >33mmol/L (600mg/dl)
Ketones Urine: negative small
Blood: 320mOsm/kg - (raised Na,
BG, urea)
Electrolytes Raised Na, BG, urea creatinine
Anion gap 7.30
normal or raised HCO3
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Treatment
Rehydration Caution!
Normal saline 1 l per hour initially
Consider strength normal saline
Potassium Only if hypokalaemic and renal functionadequate give before insulin
Insulin May be needed as slow infusion0.1 unit/kg/hour to be increased withcare if BG is slow to fall
Monitoring BG, BP, neurological function hourly untilstableElectrolytes 2-hourlyCardiac or CVP monitoring
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HHS complicationsComplication PreventionHypoglycaemia Prevent by adding glucose infusion
when glucose
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DKA and HHS prevention iskey
Identify and treat underlyingcause
Can be prevented bybetter public awareness
improved access to medicalcare
improved education in treatinghyperglycaemia during illness
emergency communicationwith healthcare provider
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Managing diabetes during illness
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Diabetes and illnesses
People with adequate glycaemiccontrol not at increased risk ofinfection
Poor metabolic control increasesrisk
- decreases immunity
- leads to persistent glycosuria anddehydration
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Impact of illness
Infective illness increased stress hormones
gluconeogenesis + insulin insensitivity hyperglycaemia + ketones
Nausea, vomiting, diarrhoea
poor gastric emptying + rapid intestinaltransit + poor food absorption
hypoglycaemia
Milder illnesses
little or no effect
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Illnesses and hyperglycaemiaGeneral management
Identify and treat cause of illness
Treat symptoms such as fever with
paracetamol Adequate fluids frequent diet
drinks
More frequent blood glucose tests Check urine for ketones
Blood ketone tests if available
Laffel et al 2005
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Insulin management
Never stop insulin (fever andstress increase insulin needs)
Continue intermediate- or long-
acting insulin
Shorter-acting insulin (soluble orrapid acting) should be adjusted
according to blood glucose values People with type 2 diabetes may
need short-term insulin treatmentif illness severe
Hanas 2004
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Algorithm for guidance
Breakfast Lunch Supper Bedtime
Usual dose (example) Soluble 10 Soluble 8 Soluble 12 NPH 24
If blood glucose is... Units of insulin reduced (-) or added (+) to usual dose
18.1 (325) + 10 units + 8 units + 12 units
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Insulin correction doses
Blood glucose >15mmol/L(270 mg/dL), ketones present
Usual insulin
PLUS
Short- or rapid-acting insulin10-20% of total daily doseevery 2-4 hours(short-actinginsulin) or every 1-2 hours(rapid-acting insulin)
Glucose tests every 1-2 hours
Eg: blood glucose 20 mmol(360 mg/dL)
normal doses insulin
Rapid acting =10 + 8 +
12 NPH = 22
Total = 52 units/day
Give 20% ~10 units of rapidacting
Give additional doses every 1 to 4 hours untilblood glucose
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Sick days and pump therapy
Rapid-acting insulin; no long-acting
If pump problem, no insulin after 3hours
Become sick very quickly
Need to carry or able to access a
new infusion set and insulin pen atall times
Need to be able to test ketones
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Insulin pump therapy
basal (25% to 100%)
Know effect of a unit of insulin onblood glucose
Correction dose for ketones up todouble usual correction
Test in 1 hour and 12 hourly
thereafter If no change suspect site problem
Use pen
Re-site cannula
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Food tolerance
Insulin must be given but may bereduced
Eg: blood glucose 10-12mmol/L
(180-216mg/dL)
About 150 ml sweetened fluidseach hour to hydrate and avoid
hypoglycaemia
If feverish, additional 150 ml low-calorie fluid each hour may be
needed for re-hydration
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If unable to tolerate food
Eg: blood glucose >15mmol/L
(270mg/dL)(additional insulin needed as above)
Give 150 ml to 300 ml of low-caloriefluid each hour for hydration and tohelp blood glucose to fall
Monitor blood glucose every 1-2hours
Food tolerance
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Provide a list of drinks easily
available in your community that
are suitable for an ill person with
diabetes who is nauseated and
unable to eat food.
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When to seek professional help
Advise to call the physician or nurse if...
Uncertain of diagnosis
Persistent vomiting or diarrhoea
(3 episodes or more within 6 hours)
Unwell for 2 days and not getting better
Blood glucose remains above 15 mmol/L(270 mg/dL) despite extra fluid andinsulin
Moderate to large ketones persist,despite extra fluid and insulin
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Hospital transfer
Transfer to hospital if...
Abdominal pain worsening
Breathing difficulty orhyperventilation
Co-existing serious diseases
Person looking increasinglyunwell/exhausted
Care-givers exhausted oruncertain of diagnosis
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Type 2 diabetes
Mr M: 20 years, type 2 diabetes
maximal sulphonylureas and metformin
twice a day intermediate acting insulin
Presented with 12 hours diarrhoea,
nausea, no appetite
What do you do?
Stop tablets, remain on insulin, or stop
insulin and remain on tablets?
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Type 2 diabetes
Metformin can aggravate gutproblems
Often easier to cease medication andcontinue insulin
Easier to control glucose levels withinsulin; may need reduced dose
Re-introduce oral medication whenfood intake normal and symptomssubside
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Type 2 diabetes
Metformin
Cease 24 hours before
surgery
Restart!
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a d SCurriculum Module III-6
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Develop clear plans for sick days
Make written guideline availableand review plans with all peoplewith diabetes regularly
Determine when healthcareprovider should be contacted oralerted
Establish blood glucose goals forsick days
Adapted from: Diab Care 2004; 27 Suppl 1
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Develop clear plans for sick days
Define how to use supplementalshort-acting insulin
Explain how to use a fluid dietwhen unable to eat
Explain what equipment is
required
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Education tips
Under-treated sick days are acommon cause of diabetic
ketoacidosis and hospitalization At each annual complication
assessment, ask your patient tosolve a sick-day scenario
Access a 24-hour hotline
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Summary diabetes and illness
Never stop insulin
Do more blood glucose tests
high blood glucose levels meansmore insulin
In case of loss of appetite, eatfoods that are easy to digest and
drink more sugar-free fluids In case of vomiting, drink frequent
small volumes of carb-containing
fluids
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Summary diabetes and illness
Call for help in case of
persistent or severe vomiting
exhaustion or confusion
rapid breathing
worsening abdominal painuncertainty
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Review question
1. Which of the following is the mostimportant ketone body in DKA?
a. Acetone
b. Acetoacetate
c. Beta-hydroxybutyrate
d. None of the above
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Review question
2. Which feature is more indicative ofHHS than DKA?
a. Extreme hyperglycaemia
b. Extreme insulin deficiency
c. Large anion gap
d. Acetone breath
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Review question
3. Which of the following strategies shouldalways be a part of the treatment plan fora person with DKA?
a. Insulin therapy and magnesiumreplacement
b. Possible insulin therapy and re-
hydration
c. Insulin therapy and re-hydration
d. Possible insulin therapy and sodiumbicarbonate replacement
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Review question
4. Which of the following strategies shouldalways be a part of the treatment plan fora person with HHS?
a. Insulin therapy and magnesiumreplacement
b. Insulin therapy and re-hydration
c. Possible insulin therapy and sodiumbicarbonate replacement
d. Possible insulin therapy and re-hydration
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Review question
5. Which electrolyte is critical to monitorduring DKA as correction of themetabolic acidosis can possibly result in
cardiac arrythmias and muscleweakness?
a. Sodium
b. Potassium
c. Acetoacetate
d. Beta-hydroxybutyrate
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Answers
1. c
2. a
3. c
4. d
5. b
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References DKA and HHS
1. Booth GL. Short-Term Clinical Consequences of diabetes. In H. Gerstein & RB Haynes(EDs.), Hamilton: BC Decker. Evidence-Based Diabetes Care 2001; 75-90.
2. Jones H, Cleave B, Fredericks C, Hamilton C, Opsteen C. Building Competency inDiabetes education: the essentials. Canadian Diabetes Association, Canada, 2001.
3. Kitabchi AE, Umpierrez GE, Murphy MB, et al. Management of hyperglycemic crises inpatients with diabetes. Diabetes Care 2001; 24(1): 131-53.
4. Kitabchi AE, Ayyagari V, Guerra SMO. The efficacy of low dose versus conventionaltherapy of insulin for treament of DKA. Ann Int Med 1976; 84: 633-8.
5. American Diabetes Association. Hyperglycemic crisis in patients with diabetes.Diabetes Care 2001; 26(S1): S109-17.
6. Meltzer S, Yale JF, Belton AB, Clement M. Eds. Practical Diabetes Management;Clinical support for primary care physicians 5th ed.Canadian Diabetes Association,Canada, 2004.
7. Davidson MB. Hyperglycemia. In: Franz MJ, ed. A Core Curriculum for DiabetesEducation: Diabetes and Complications. 4th ed. Chicago: American Association of
Diabetes Educators 2001; 23.
8. Joslins Diabetes Mellitus. Eds Kahn CR,Weir GC et al. Publ Lippincott Williams &Wilkins, Philadelphia, 2005; 53.
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References managing illness
1. Hyperglycemic crises in diabetes. ADA position statement. Diab Care 2004; 27(Suppl 1).
2. Hanas R. Type 1 diabetes in children, adolescents and young adults. 2nd edition2004. Publ Class Publishing, London
3. Laffel L, Pasquarello C, Lawlor M. Treatment of the child and adolescent withdiabetes. Chap 35 in Joslins Textbook Diabetes. Publ Lippincott Williams &Wilkins, Philadelphia, 2005.